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Morphologic features of unstable atherothrombotic plaques underlying acute coronary syndromes
1Institute of Pathology, Odense, Denmark.
Insights
Unstable angina signals rapid coronary artery disease progression. Therapies targeting plaque disruption, thrombosis, and vasospasm can prevent progression to myocardial infarction or sudden death.
Area of Science:
- Cardiovascular Medicine
- Pathology
- Interventional Cardiology
Background:
- Unstable angina is a key indicator of rapidly progressing coronary artery disease.
- Autopsy studies reveal unstable atherothrombotic coronary lesions in patients with unstable angina.
- These lesions feature ruptured plaques with hemorrhage and luminal thrombosis.
Purpose of the Study:
- To elucidate the pathological mechanisms underlying unstable angina and its progression.
- To understand the role of dynamic thrombosis in acute coronary events.
- To identify therapeutic targets for preventing myocardial infarction and sudden death.
Main Methods:
- Pathological examination of coronary lesions in autopsy cases.
- Correlation of lesion morphology with clinical presentation of unstable angina.
- Analysis of thrombus characteristics and myocardial microinfarcts.
Main Results:
- Unstable atherothrombotic lesions with plaque rupture and thrombosis are common in unstable angina.
- Occlusive thrombi are more frequent with increasing stenosis severity (>75%).
- Evidence of episodic thrombus growth and peripheral embolization (microemboli/microinfarcts) was observed.
Conclusions:
- Unstable angina signifies a dynamic process of plaque rupture and thrombosis.
- Progression to myocardial infarction or sudden death is linked to this "dynamic thrombosis" and vasospasm.
- Timely therapies targeting atherosclerosis, plaque disruption, thrombosis, and vasospasm can be preventative.
Abstract:
Unstable angina appears to be a good clinical marker for rapidly progressing coronary artery disease. Pathologically, an unstable atherothrombotic coronary lesion, represented by a raised atherosclerotic plaque with ruptured surface causing variable degree of hemorrhage into the plaque and luminal thrombosis (rapid plaque progression), usually is present in patients at autopsy after a period of unstable angina. The thrombus at the rupture site may be mural and limited (just sealing the rupture) or occlusive, depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less than 75% stenosis (histologic cross-sectional area reduction), but it is found with increasing frequency when severity of stenosis increases beyond 75%. Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits, and microemboli/microinfarcts are frequently found in the myocardium downstream to coronary thrombi, indicating intermittent thrombus fragmentation with peripheral embolization. Such a "dynamic thrombosis" (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other thrombus-related acute coronary events: myocardial infarction or sudden death. Accordingly, progression of unstable angina to myocardial infarction or sudden death should, in principle, be preventable by the correct timing of current available therapies aimed to prevent or eliminate (1) the chronic atherosclerotic obstruction, (2) the acute plaque disruption, (3) luminal thrombosis, and (4) vasospasm.